In AML cell lines, Apatinib alone and in combination with HHT were studied. As a result of suppressing VEGFR2 expression and downstream signaling cascades, such as PI3K, MAPK, and STAT3, Apatinib and HHT inhibited cell proliferation, reduced the capacity for colony formation, and induced apoptosis and cell cycle arrest in AML cells [324]. The gene discussed is KDR; the disease is acute myeloid leukemia.